I propose to elucidate the mechanisms that regulate vascularization during would healing. Vasculogenesis is an important event of early wound healing, delivering nutrients, oxygen and inflammatory cells (and possibly precursor stem cells) to the wound site. However, during the resolving phase of repair, most of the new vessels involute. Excessive vasculature prevents the maturation of the dermis to a relatively acellular barrier. While many groups are examining the initiating of new vessels, few are looking at the stop signals that limit the neovasculature. Previous work in my mentor's laboratory identified a class of chemokines that act as stop signals for fibroplasia during the resolving phase of wound healing. For this study, I hypothesize that these ELR-negative CXC chemokines IP-10 and/or Mig also prevent excessive vascularization. I will first verify that endothelial cell migration is inhibited as reported in the literature. Then I will identify the pathway(s) through which IP-10 and/or Mig inhibits endothelial cell migration/proliferation. I also will investigate whether the CXC chemokine receptor 3 is upregulated on microvascular endothelial cells at different stages of wound healing. Lastly, we will determine the signals that induce the production and release of IP-10 and Mig from cells during wound healing. This study will provide potential new targets to promote or limit vascular development in tissue and contribute to our ability to engineer tissues with appropriate microvasculature.